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从微小RNA视角看卡波西肉瘤相关疱疹病毒与宿主的相互作用

Looking at Kaposi's Sarcoma-Associated Herpesvirus-Host Interactions from a microRNA Viewpoint.

作者信息

Liang Deguang, Lin Xianzhi, Lan Ke

机构信息

Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences Shanghai, China.

出版信息

Front Microbiol. 2012 Jan 11;2:271. doi: 10.3389/fmicb.2011.00271. eCollection 2011.

DOI:10.3389/fmicb.2011.00271
PMID:22275910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3258008/
Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV), also called human herpesvirus 8, belongs to the gamma herpesviruses and is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma, and some types of multicentric Castleman's disease. In vivo, KSHV mainly infects B cells and endothelial cells. The interactions between KSHV and its host cells determine the outcome of viral infection and subsequent viral pathogenesis. MicroRNAs (miRNAs) are small, non-coding RNAs that are important in fine-tuning cellular signaling. During infection, KSHV modulates the expression profiles and/or functions of a number of host miRNAs, for example hsa-miR-132 and hsa-miR-146a. Meanwhile, KSHV itself encodes 12 pre-miRNAs, including miR-K12-11, which is the functional ortholog of the host miR-155. A number of cellular and viral targets of deregulated cellular miRNAs and viral miRNAs are found in KSHV-infected cells, which suggests that miRNAs may be important in mediating KSHV-host interactions. In this review, we summarize our current understanding of how KSHV modulates the expression and/or functions of host miRNAs; we review in detail the functions of miR-K12-11 as the ortholog of miR-155; and we examine the functions of viral miRNAs in KSHV life cycle control, immune evasion, and pathogenesis.

摘要

卡波西肉瘤相关疱疹病毒(KSHV),也称为人类疱疹病毒8型,属于γ疱疹病毒,是卡波西肉瘤、原发性渗出性淋巴瘤和某些类型多中心性Castleman病的病原体。在体内,KSHV主要感染B细胞和内皮细胞。KSHV与其宿主细胞之间的相互作用决定了病毒感染的结果以及随后的病毒发病机制。微小RNA(miRNA)是小的非编码RNA,在微调细胞信号传导中起重要作用。在感染过程中,KSHV调节许多宿主miRNA的表达谱和/或功能,例如hsa-miR-132和hsa-miR-146a。同时,KSHV本身编码12种前体miRNA,包括miR-K12-11,它是宿主miR-155的功能同源物。在KSHV感染的细胞中发现了许多失调的细胞miRNA和病毒miRNA的细胞和病毒靶标,这表明miRNA可能在介导KSHV与宿主的相互作用中起重要作用。在这篇综述中,我们总结了我们目前对KSHV如何调节宿主miRNA的表达和/或功能的理解;我们详细回顾了miR-K12-11作为miR-155同源物的功能;并且我们研究了病毒miRNA在KSHV生命周期控制、免疫逃逸和发病机制中的功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d9a/3258008/af3c45da6cfd/fmicb-02-00271-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d9a/3258008/d3d0a8692106/fmicb-02-00271-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d9a/3258008/af3c45da6cfd/fmicb-02-00271-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d9a/3258008/d3d0a8692106/fmicb-02-00271-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d9a/3258008/af3c45da6cfd/fmicb-02-00271-g002.jpg

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本文引用的文献

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Kaposi's sarcoma-associated herpesvirus-encoded microRNA miR-K12-11 attenuates transforming growth factor beta signaling through suppression of SMAD5.卡波西肉瘤相关疱疹病毒编码的 microRNA miR-K12-11 通过抑制 SMAD5 来减弱转化生长因子 β 信号通路。
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